PPAR-α通过PI3K/Akt/FoxO1信号通路的负性调控心肌细胞肥大  

Negative Regulation of PPAR-α on Cardiomyocyte Hypertrophy through PI3K/Akt/FoxO1 Signaling Pathway

作　　者：潘勇权 胡惠军[1] 古彩红[1] 陈思琦[1] 范晓娟 林小龙[1] 

机构地区：[1]广东省惠州市第三人民医院病理科,广东惠州516002

出　　处：《临床医学工程》2018年第1期23-24,共2页Clinical Medicine & Engineering

基　　金：广东省医学科研基金项目(项目编号:A2015620);惠州市科技计划项目(项目编号:2016Y155)

摘　　要：目的观察PPAR-α对心肌细胞肥大负性调控时,机体中PI3K/Akt/Fox O1信号通路的变化情况。方法实验小鼠以异丙肾上腺素诱导心肌细胞肥大,使用实时定量聚合酶链式反应检测Fox O1 m RNA、PPAR-α表达水平,同时应用Feno预处理后观察Fox O1 m RNA、PPAR-α表达水平变化。结果异丙肾上腺素诱导后,心肌细胞中的PPAR-αm RNA、Fox O1 m RNA水平降低。Feno能抑制心肌肥大细胞表面积增加,RNAi通过PPAR-αm RNA使心肌肥大细胞表面积增加,以PI3K抑制剂LY处理心肌细胞,Fox O1 m RNA表达增加。结论 PPAR-α对心肌细胞肥大负调控与PI3K/Akt通路抑制、增加Fox O1表达有关。Objective To observe the changes of PI3K/Akt/FoxO1 signaling pathway during the negative regulation of PPAR-α on cardiomyocyte hypertrophy. Methods The cardiomyocyte hypertrophy of experimental mice was induced by isoprenaline. The FoxO1 mRNA and PPAR-α expression levels were detected by real-time quantitative polymerase chain reaction. At the same time, the changes of FoxO1 mRNA and PPAR-α expression levels were observed after pretreatment with Feno. Results After isoprenaline induction, the PPAR-α mRNA and FoxO1 mRNA levels decreased in cardiomyocytes. Feno could inhibit the increase of cardiomyocyte surface area. RNAi could improve the cardiomyocyte surface area through PPAR-α mRNA. The FoxOl mRNA expression increased when the cardiomyocytes were treated with PI3K inhibitor of LY. Conclusions The negative regulation of PPAR-α on cardiomyocyte hypertrophy is related to the inhibition of PI3K/Akt pathway and the increase of FoxO 1 expression.

关 键 词：PPAR—α FOXO1 心肌细胞肥大 PI3K/AKT 

分 类 号：R542.2[医药卫生—心血管疾病]